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[Intracranial calcifications--seizures--celiac disease: a case presentation]
G Della Cella1, C Beluschi, F Cipollina
1Divisione Pediatria, Ospedale di Chiavari (GE), Italia.
Insights
This case study highlights a boy with coeliac disease and seizure disorder. Intracranial calcifications and neurological symptoms improved with a gluten-free diet, emphasizing the link between coeliac disease and neurological conditions.
Area of Science:
- Neurology
- Gastroenterology
- Pediatrics
Background:
- Coeliac disease is an autoimmune disorder triggered by gluten ingestion.
- Neurological manifestations can occur in coeliac disease, though less commonly.
- This case explores the complex interplay between coeliac disease and neurological symptoms in a pediatric patient.
Observation:
- A 4-year-old boy presented with seizures and fatty stools, leading to a coeliac disease diagnosis via jejunum biopsy.
- Neurological symptoms, including generalized convulsions, initially improved on a gluten-free diet.
- Intracranial calcifications, particularly in the occipital region, were identified via CT scans during follow-up.
Findings:
- Discontinuation of the gluten-free diet led to the recurrence of seizures.
- Low folic acid levels were noted when dietary adherence was poor.
- Neurological symptoms evolved from seizures to daily 'mind-failures' during puberty, persisting into adulthood.
Implications:
- This case underscores the importance of considering coeliac disease in children with unexplained neurological disorders.
- Intracranial calcifications may be a significant, though not fully understood, feature associated with coeliac disease.
- Long-term management requires vigilant dietary adherence and neurological monitoring for patients with coeliac disease and associated neurological complications.
Abstract:
The Authors report a case of coeliac disease which first appeared in a boy of 4, suffering from a seizure disorder. The bulky mass of fatty faeces led towards gastroenteric investigations (xylose-test, jejunum biopsy). The atrophy of the villi was clearly shown by the biopsy and a coeliac disease was easily diagnosed. The boy was prescribed a coeliac diet and no fits of generalized convulsions occurred during three years follow-up. Yet, while he was given a challenge free-diet, they started to occur. A computerized axial tomography (TAC) carried out when he was eight and another when fifteen, evidenced bilateral, intracranial calcifications, cortical-subcortical, in the blood vessels, symmetrically located in the occipital region. The anticonvulsive therapy, started when he was 4, has never been interrupted. Now A.M. is 21 and still following an anticonvulsive polytherapy. Many tests were performed. The result of folic acid dosage carried out when he was 16, and badly follow a coeliac diet, was less than 2 ng/ml. A modification in the neurological symptomatology was noted during his puberal phase: fits of convulsions changed into daily crises of mind-failures. This feature is still present in his adult age. The case is reported for its clinical characteristics of neurological symptomatology associated with coeliac disease. The iconographical documentation evidences endocranial calcifications frequently connected with coeliac disease.